Chapter 10: Abdominal Emergencies. - Tripod.com

96 Pages·2005·0.18 MB·English

C J Mieny, U Mennen: Principles of Surgical Patient Care - Volume II
Chapter 10: Abdominal Emergencies
Chapter 10.1: Peritoninitis and Intra-Abdominal Abscess
J E J Krige
Intra-abdominal sepsis, including peritonitis and abscess formation, presents serious
and potentially life-threatening events in the management of surgical patients with
significant resultant morbidity and mortality. Twenty percent of patients presenting with
generalized suppurative peritonitis and over 50% of high-risk patients with postoperative
intra-abdominal sepsis die despite intensive treatment. Major recent advances have
occurred in the conceptual understanding of the pathogenesis, diagnostic methodology,
antibiotic therapy and application of non-invasive technology in intra-abdominal sepsis. As
a consequence, the management of intra-abdominal infection requires a careful
interdisciplinary approach, with close collaboration between surgeon, physician,
radiologist, bacteriologist and anaesthetist.
This chapter outlines the relevant anatomy and physiology, pathogenesis, clinical
features, diagnostic approach and management of primary and secondary bacterial
peritonitis and intra-abdominal abscess.
Anatomy
The peritoneum is the larges serous membrane in the body and consists of a single
layer of mesothelial cells supported on a connective tissue base. The parietal peritoneum
lines the anterior, lateral and posterior abdominal walls, the undersurface of the diaphragm
and the pelvis and is reinforced by transversalis fascia. The visceral peritoneum is
reflected onto the intra-abdominal viscera, mesentery and omentum, creating a closed
cavity except for the open end of the fallopian tubes. Although the parietal and visceral
surfaces are part of the same membrane, the distinction is relevant with regard to
differences in sensory innervation. The peritoneal cavity forms the potential space between
the parietal and visceral layers and is divided into the general peritoneal cavity or greater
sac, and the lesser sac which communicates via the foramen of Winslow. The anatomic
surface area of the peritoneum in adults is about 1.7 m2 and approximates the total body
surface area.
The parietal peritoneum has a somatic afferent nerve supply and is sensitive to all
forms of stimuli. Irritation of the parietal peritoneum produces sharp, well localized,
discriminate pain with tenderness, involuntary guarding and rigidity of the abdominal
muscles if the stimulus is sufficiently intense. The parietal peritoneum on the undersurface
of the diaphragm is supplied centrally by the phrenic nerves and peripherally by lower
intercostal nerves. Irritation of the peritoneum over the central portion of the diaphragm
results in referred pain in the distribution of the cutaneous branches of the third, fourth
and fifth cervical nerves over the shoulder region.
The visceral peritoneum receives afferent innervation only from the autonomic
nervous system and is relatively insensitive to tactile, thermal and chemical stimuli.
Stimuli from the visceral peritoneum characteristically are poorly localized and are
perceived as a dull pain. The visceral afferent nerves have no receptors to mediate pain
and temperature, but are sensitive to bowel ischemia and distention or traction on the
mesentery.
Physiology
The peritoneum consists of a single surface layer of mesothelial cells supported on
a basement membrane and a deeper well-vascularized connective tissue layer containing
collagen and elastic fibres, fat cells, reticulum cells and macrophages. The peritoneal
cavity contains less than 50 mL of clear fluid consisting of water, electrolytes and solutes
derived from interstitial fluid and plasma. Normal peritoneal fluid has a specific gravity of
less than 1016 and less than 3 grams per mL of protein, predominantly albumen.
Fibrinogen is not present and the fluid will not clot. Much of the peritoneal membrane
acts as a passive, semi-permeable barrier to the bidirectional diffusion of water and most
solutes. Normal peritoneal fluid contains less than 3000 cells per cubic mL with 50%
lymphocytes, 40% macrophages, a few eosinophils, mast cells and occasional
desquamated mesothelial cells. Bacteria are absent. Peritoneal fluid has minimal
antibacterial activity, mediated both via the complement system and the lymphocyte
population in the fluid. The number of granulocytes is significantly increased in the
presence of inflammation. Peritoneal aspiration may be of value for culture and chemical
analysis to facilitate the diagnosis of inflammatory conditions, tumours or intraperitoneal
trauma. The principal route of absorption and clearance of fluids and particulate matter
from the peritoneal cavity is by lymphatics. Reverse flow is prevented by one-way valves
within the thoracic lymphatic system. Experimentally, particulate matter including red cells
and bacteria, is recoverable from the thoracic lymph within 6 minutes and from the blood
within 12 minutes after intraperitoneal injection. Absorption of fluid by the diaphragmatic
lymphatics produces a cephalad flow of peritoneal fluid which is promoted by increased
respiratory movement. The rapid peritoneal clearance of particulate matter and fluid,
functions as the essential first line of defence following initial peritoneal contamination.
Definition
Peritonitis is the acute inflammatory response of the visceral and parietal
peritoneum to bacterial, chemical, radiation or foreign body injury. The two major clinical
categories of peritonitis are based on aetiology:
- Primary peritonitis is an infection of the peritoneum occurring de novo without
obvious intra-abdominal pathology.
- Secondary bacterial peritonitis is a purulent inflammation of the peritoneum
due to contamination following a complication of a pre-existing primary intra-abdominal
process such as perforated peptic ulcer, ruptured appendix or a disrupted anastomotic
suture line.
Secondary bacterial peritonitis is more common and of greater surgical significance
than primary peritonitis; accurate differentiation between the two types is crucial for
optimal management.
Primary Peritonitis in Children
Primary peritonitis is uncommon, accounting for less than 1% of all cases of
peritonitis and predominantly affects girls under 10 years. The bacteria involved are
primarily pneumococci and Group A streptococci. Less commonly, gram-negative bacilli
and Group B streptococci are found. A useful diagnostic feature in differentiating the
usually monobacterial spontaneous peritonitis from the polymicrobial flora of secondary
peritonitis is the single species of bacteria cultured. About one half of cases of
pneumococcal peritonitis occur in children with nephrosis. The causative bacteria gain
access to the peritoneum by a haematogenous route or, uncommonly, via the fallopian
tubes.
The clinical manifestations are those of acute diffuse peritonitis. A pre-existing
upper respiratory infection, pneumonia or otitis media may mask the initial onset of
peritonitis. Severe, generalized abdominal pain is the predominant symptom. High fever,
often with chills, irritability, vomiting and diarrhoea, is common. On examination, the
child appears ill, pyrexial with a temperature of 40 °C and an elevated pulse rate. The
abdomen is diffusely tender and ascites with shifting dullness may be demonstrated.
Bowel sounds are hypoactive or absent. The white blood count reveals a leucocytosis of
20000-40000/mm3 with a polymorphonuclear predominance and a shift to the left. Heavy
albuminuria is present in cases superimposed on nephrosis. Blood culture is usually
positive for streptococci or pneumococci. A peritoneal aspirate under local anaesthesia
with an immediate gram stain is important to differentiate primary peritonitis in which
surgical intervention is contra-indicated from peritonitis secondary to a perforated
appendix where prompt surgery is necessary. If only cocci are seen on the smear,
conservative therapy is appropriate. A mixed bacterial flora on the smear demands an
exploratory laparotomy.
Primary Peritonitis in Adults
Spontaneous bacterial peritonitis (SBP) is an infective complication caused by
enteric organisms and usually occurs in alcoholic cirrhotic patients with ascites.
Characteristically, the patient presents with fever, abdominal pain, reduced or absent bowel
sounds and encephalopathy in the presence of gross ascites. The presentation may be
subclinical and subtle and the only clinical manifestation in a known cirrhotic may be
unexplained deterioration in liver function, progressive encephalopathy or diminishing
renal function. A diagnostic ascitic tap is necessary to determine the presence of bacteria,
neutrophils, protein, glucose and pH of the ascitic fluid. Gram stains are positive,
however, only in one-third of culture proven cases. Careful aerobic and anaerobic cultures
isolate a single organism in 80% of patients with SBP; the most frequent organisms
recovered are E. coli and pneumococci. Anaerobes are virtually never isolated. The ascitic
fluid WBC is generally > 500/mm3 with more than 75 neutrophils/mm3. A peritoneal
acidosis with a pH of less than 7.3 is due to lactic acid production by the infecting
organisms. While the bacterial infection may be effectively treated with suitable
antibiotics, the prognosis is poor and mortality exceeds 80% due to progressive liver
decompensation, renal failure, encephalopathy and haemorrhage.
Secondary Bacterial Peritonitis
Secondary bacterial peritonitis is an acute suppurative inflammatory process of the
peritoneal cavity arising as a consequence of:
- primary disease of the abdominal viscera
- penetrating or blunt trauma
- previous intra-abdominal surgery.
Aetiology
Secondary peritonitis may complicate almost any abdominal condition including
inflammatory, traumatic, obstructive or neoplastic processes (table 10.1.1). Perforation
following appendicitis or diverticulitis is the most common cause of acute suppurative
bacterial peritonitis. Delayed treatment of duodenal and gastric perforations are further
common causes of bacterial peritonitis. Gangrene of the bowel, either from strangulation
or ischaemia, remains an important cause of peritonitis. Pelvic peritonitis often
accompanies pelvic inflammatory disease, especially if infection of the fallopian tubes is
severe, but seldom progresses to frank generalized peritonitis. Penetrating or blunt
abdominal trauma may cause contamination of the peritoneal cavity and subsequent
widespread inflammation. Some degree of inflammation follows every surgical procedure
within the peritoneal cavity. Due to inevitable minor contamination from room air, poor
surgical technique, glove perforation or spillage during resection or manipulation. Such
contamination is nearly always contained by the protective mechanisms within the
peritoneal cavity, but gross contamination, virulent organisms or immune compromise may
result in clinically significant peritonitis.
Pathogenesis
The initial local responses of the peritoneum to contamination or injury are
vascular dilatation, hyperaemia and increased capillary permeability, followed by
transudation of fluid from the vascular and interstitial spaces. Fluid containing opsonins,
polymorphonuclear leucocytes and macrophages accumulates in the involved tissues and
the free peritoneal space. Phagocytosis of bacteria and foreign material is the major local
peritoneal defence mechanism and the peritoneal exudate contains antibodies and
complement which enhance aggregation, adherence and engulfment of micro-organisms, in
addition to promoting chemotaxis and diapedes of white cells. The peritoneum loses its
normal sheen and acquires a dull ground-glass appearance due to deposition of fibrinogen.
The release of tissue thromboplastin converts fibrinogen to fibrin. Normal peritoneum,
however, has a fibrinolytic capacity due to plasminogen activator present in mesothelial
cells. Injury to the peritoneum produces an inhibition in fibrinolytic activity which permits
the development of fibrinous adhesions that wall off and surround the inflamed area or
injury. This abundant fibroblastic exudate aids specific humoral and cellular immune
defence mechanisms in localizing the inflammatory process. Further restriction of the
inflammatory process is due to peritoneal and omental tissue adaptation with adhesions
between loops of bowel and the parietal wall with migration of the greater omentum into
the area of inflammation to further compartmentalize the infective process. The regional
lymphatic circulation provides an important peritoneal defence mechanism by absorption
of bacteria through the lymphatic system present beneath the diaphragmatic mesothelium.
Bacteria removed via the lymphatics are filtered by the thoracic lymph nodes or, once in
the systemic circulation, are eliminated by the reticulo-endothelial cells in the liver and
spleen.
Table 10.1.1. Aetiology of Secondary Bacterial Peritonitis
1. Inflammatory
1. Inflammatory
a. Intestine
- Diverticulitis with perforation
- Appendicits
- Meckel's diverticulitis
- Necrotizing enterocolitis
- Ulcerative colitis
- Amoebic colitis
b. Visceral
- Salpingitis
- Empyema of gallbladder
- Necrotizing pancreatitis
- Liver abscess
2. Strangulation obstruction
a. Small bowel
- Closed-loop adhesive obstruction
- Hernia: internal, external
- Volvulus with strangulation
- Intussusception
b. Colon
- Volvulus: sigmoid, caecal
- Closed loop obstruction (neoplasm, diverticulum)
3. Trauma
a. Blunt rupture of viscus: stomach, small bowel, colon
b. Penetrating
c. Iatrogenic
- endoscopy/biopsy
- anastomotic disruption
4. Perforation
a. Neplasms: gastric, colon carcinoma
b. Foreign body
c. Duodenal, gastic ulcer
5. Vascular
a. Mesenteric embolus
b. Ischaemic colitis.
If the peritoneal defences are able to contain the inflammatory process, the disease
may end by resolution. A second possible outcome is localization of the process with
contained suppuration and abscess formation. If the peritoneal and systemic defence
mechanisms are unable to localize the inflammation, generalized suppurative peritonitis
occurs. The factors favouring spread of the inflammatory process are:
--> overwhelming or continued bacterial contamination
--> virulence and synergistic bacterial action
--> presence of foreign bodies or adjuvant factors deleterious to resolution of the
inflammation.
Continuing contamination of the peritoneal cavity occurring with free anterior
perforation of a duodenal ulcer or perforation secondary to an obstructive colonic
carcinoma results in rapid dissemination of bacteria throughout the peritoneal cavity. The
volume and rate of spill are critical factors. Intra-abdominal spread of contamination is
promoted by the peristaltic movement of the viscera and by diaphragmatic motion
producing a cyclic pressure differential between the subphrenic space and the peritoneal
cavity. The subphrenic area is contaminated by movement of bacteria into the potential
space by the negative suction of the diaphragm during respiration. In addition, the effect
of gravity in the recumber patient allows fluid to drain into the most dependent spaces.
A mixed bacterial flora is usually found in acute suppurative peritonitis after
secondary contamination from the intestinal tract. The most common organisms are
aerobic coliforms, in particular E. coli, Proteus, Klebsiella, and aerobes including
Bacteroids, anaerobic cocci and Clostridia (table 10.1.2).
Table 10.1.2. Bacteriology of Secondary Peritonitis
Aerobic Bacteria
--> E. col 60
--> Streptococci 28
--> Enterobacter/Klebsiella 26
--> Proteus 22
--> Enterococci 17
--> Pseudomonas 8
--> Staphylococci 7
--> Candida 2
Anaerobic Bacteria
--> Bacteroides 72
--> B. fragilis 38
--> Eubacteria 34
--> Clostridia 17
--> Peptostreptococcus 14
--> Peptococci 11.
All these bacteria are potentially lethal pathogens in the human. The mixed
aerobic-anaerobic faecal flora commonly found in peritonitis frequently acts
synergistically. Particular combinations such as E. coli and B. fragilis produce a mortality
rate significantly greater than the mortality rate of each organism alone. The mortality rate
resulting from peritonitis is in part a dose-dependent phenomenon correlating directly
directly with the number of pathogenic bacteria introduced into the peritoneal cavity. In
duodenal perforations, few bacteria are cultured initially, but bacterial proliferation
increases significantly after six hours. Perforation of obstructed distal small bowel or
colon, however, results in immediate gross contamination. The site of the gastrointestinal
perforation and, by inference, the number of bacteria escaping from the lumen are
therefore critical determinants in the risk of subsequent infection. Not all organisms
cultured from the intraperitoneal fluid, however, have equivalent virulence. E. coli and B.
fragilis are regarded as the major pathogens in intraabdominal sepsis since they are found
most often in positive blood cultures.
Certain adjuvant substances increase the lethality of peritonitis, ie, the presence of
necrotic tissue in the peritoneal cavity significantly enhances the risk of continuing
infection. The virulence of contaminating micro-organisms is further enhanced by mucus,
bile, barium sulphate and haemoglobin. This characteristic is attributed to the detrimental
effect of the adjuvant on defence mechanisms, especially phagocytosis. The co-existence
of haemoglobin and bacterial inoculum within the peritoneal cavity produces an increased
susceptibility to the micro-organisms, since clearance of bacteria from the peritoneal cavity
is inhibited by haemoglobin. Haemoglobin specifically inhibits intraperitoneal chemotaxis
of neutrophils, phagocytosis and intracellular killing of bacteria. Haemoglobin also
interferes with lymphatic absorption of bacteria and exerts and additional local toxic effect
after degradation.
Pathophysiology
Peritonitis produces profound physiological alterations both locally within the
abdominal cavity and also systemically affecting the cardiovascular, respiratory, renal and
neuro-endocrine system.
Fluid Shifts
The peritoneum reacts to inflammation by vascular dilatation, hyperaemia and
exudation of fluid from the vascular space into the free peritoneal cavity, the loose
connective tissues beneath the mesothelium of viscera and mesenteries as oedema fluid
and into the lumen of the atonic dilated gastrointestinal tract. This translocation of water,
electrolytes and protein into the sequestrated third space effectively removes fluid from the
body economy. The rate of fluid loss is proportional to the surface area of peritoneum
involved in the inflammatory process and with extensive peritonitis, may reach 4-6 L in
24 hours.
Ileus
Generalized peritonitis produces an inhibition of intestinal motility with resultant
dynamic ileus. Distention of the bowel with unabsorbed fluid and gas, aggravated by
relative mural ischaemia if intraluminal pressure exceeds capillary perfusion pressure,
permits bacteria to penetrate the mucosal barrier and enter the vascular compartment.
Endocrine Response
Peritonitis results in a major systemic stress producing a vigorous response from
the pituitary-adrenal axis. Adrenal medullary secretion of catecholamines is in large part
responsible for the vasoconstriction, tachycardia and sweating accompanying the initial
response to peritonitis. Aldosterone secretion increases as a response to hypovolaemia and
further aggravates potassium loss and sodium retention. Release of antidiuretic hormone
results in renal conservation of water which may exceed sodium retention with consequent
dilutional hypotonicity of plasma sodium.
Cardiovascular System
Loss of extracellular fluid volume depletes central venous return, lowering cardiac
output and increasing heart rate. Compensatory vasoconstriction results in an increased
total peripheral resistance to maintain blood pressure and cardiac and cerebral perfusion
pressures. Decreased perfusion and oxygenation to the splanchnic bed, kidneys and
inactive muscles result in anaerobic glycolysis with progressive accumulation in lactic
acid.
Metabolic acidosis is aggravated by decreased renal clearance, secondary to
reduced renal perfusion. If acidosis progresses, depression of cardiac contractility further
decreases cardiac output.
Respiratory System
Demands on the respiratory system increase significantly in peritonitis, with a
decrease in total respiratory capacity. Abdominal distention secondary to ileus causes an
elevation and restriction of diaphragmatic movement. Respiratory restriction, fatigue and
inefficient respiratory effort diminish ventilatory volume with ensuing atelectasis which
may progress to ventilation-perfusion imbalance, intrapulmonary arteriovenous shunting
and peripheral hypoxaemia.
Kidneys
Renal changes induced by peritonitis are primarily a reflection of hypovolaemia,
reduced cardiac output and increased secretion of aldosterone and antidiuretic hormone.
Renal blood flow, glomerular filtration and urine volume are reduced. Aldosterone
promotes sodium retention and antidiuretic hormone results in increased reabsorption of
water from the distal tubules with a further decrease in urine output.
Protein catabolism progresses during the duration of peritonitis and serum albument
concentrations decrease with further loss into the peritoneal cavity. Hepatic glycogen
stores are depleted. The net effect of these metabolic changes in the body results in a
significant energy deficit.
Clinical Features
The predominant symptom in peritonitis is abdominal pain aggravated by any
movement, including respiration. Perforation of a peptic ulcer with massive contamination
of gastric contents produces sudden onset of epigastric pain with rapid spread to involve
the entire abdomen corresponding to spread of acid-pepsin throughout the peritoneal
cavity. The spread of pain from lesions such as a perforated appendix or a diverticular
abscess is more gradual corresponding to progression of bacterial inflammation. Anorexia,
nausea and vomiting commonly accompany peritonitis. Patients may complain of feeling
feverish, sometimes with rigors, and of thirst and decreased urine output. Other symptoms
of adynamic ileus produced by the peritonitis are the inability to pass faeces or flatus and
abdominal distention.
Physical Findings
Patients characteristically lie quietly in bed with the knees flexed and frequently
shallow respiration. With advancing infection, respiration becomes more rapid as the
demand for tissue oxygen utilization increases and acidosis worsens. Respiration is
primarily intercostal since diaphragmatic movement worsens pain. Body temperature
elevation in peritonitis is usually 39 °C to 40 °C but may reach 42 °C in overwhelming
sepsis. Subnormal temperatures are seen in the early stages of chemical peritonitis and late
in septic shock, where progressive peripheral hypothermia is a grave sign.
Immunosuppressed patients do not show a marked febrile response; fever is usually higher
and more spiking in character in younger, healthier patients than in the elderly. Increasing
tachycardia with weak peripheral pulses reflects the circulatory effects of both
hypovolaemia and toxaemia. With progression of peritonitis, blood pressure may be
significantly reduced due to septic shock.
Abdominal examination elicits generalized tenderness with reflex guarding of the
adominal muscles. Extensive abdominal hyper-resonance due to gaseous bowel distention
may be demonstrated by percussion. Pneumo-peritoneum from a ruptured hollow viscus
may produce decreased liver dullness. Bowel sounds are audible on auscultation in the
initial stages of peritonitis, but with spread of inflammation the silen abdomen of
adynamic ileus supervenes. Rectal and vaginal examinations are an essential part of the
diagnostic procedure and must not be omitted in evaluating the patient with signs of
peritonitis. Anterior tenderness on pelvic examination, or the presence of a mass in the
rectouterine and rectovesical pouch may provide an important clue to pelvic sepsis.
Palpation of the cervix with excitation tenderness suggests the presence of inflammation in
the uterus and adnexae, while examination of material on the glove may give a clue to the
etiology of the process.
Diagnostic Studies
A leucocytosis between 15000 and 20000 per mm3 is usual in peritonitis with the
differential count showing a polymorphonuclear predominance and shift to the left. Blood
chemistry shows variable degrees of haemoconcentration and dehydration. Acidosis, both
metabolic and respiratory, is present in severe and late cases. Urinalysis serves to exclude
infection of the urinary tract as a source of abdominal pain. An increased serum amylase
may indicate pancreatitis or a surgically correctable cause of hyperamylasemia including
perforated duodenal ulcer or strangulated small bowel.
The X-ray findings of peritonitis may be non-specific with features of a paralytic
ileus with distention of both small intestine and colon. Inflammatory exudate and oedema
of the bowel wall produces widening of the space between adjacent bowel loops and
peritoneal fat lines and psoas shadows are obliterated. Free air may be visible beneath the
right diaphragm and occasionally beneath the left hemidiaphragm. An intra-abdominal
abscess may be detected by extraluminal airfluid levels or by the mottled soap-bubble
appearance of an anaerobic abscess. In advanced cases with bowel necrosis, intramural gas
may be seen in the intestinal wall. Portal vein gas is a late sign of bowel infarction in
adults and occurs in infants with necrotising enterocolitis.
Management of Bacterial Peritonitis
Every patient with acute peritonitis is potentially critically ill and requires the rapid
institution of physiological monitoring and aggressive treatment. The essential elements of
management in sequence are fluid resuscitation, antibiotic administration, decompression
of the gastrointestinal tract and, when appropriate, exploratory laparotomy. The patient
with established peritonitis requires repeated systematic clinical evaluation with frequent
determination of blood pressure, pulse, central venous pressure, and urine output with
specific gravity. In older patients and in younger patients with cardiovascular compromise,
a Swan-Ganz pulmonary artery balloon catheter should be inserted to determine pulmonary
artery and wedged pulmonary artery pressures. A Foley catheter is essential to determine
hourly urine output and a nasogastric tube should be inserted for decompression of the
stomach to avoid vomiting and further progression of intestinal distention. Laboratory tests
should be obtained for haematocrit, blood count, electrolytes, urea and creatinine, amylase
and liver function. Respiratory function is assessed with repeated arterial blood gas
determination, while in critically ill patients, a radial arterial line provides access for
arterial samples for blood gas analysis and a constant mean arterial pressure record.
Hypoxaemia is a frequent complication in diffuse peritonitis due to increased
permeability of the pulmonary vasculature with transudation of fluid into alveoli and
decreased oxygen exchange and is treated by increasing inspired oxygen using a 40%
ventimask and assessing response with regular blood gas analysis. Endotracheal intubation
and positive pressure respiration with a volume-controlled pressure respiration are
indicated if the patient remains hypoxic.
A critical caveat in the treatment of peritonitis is the frequent underestimation of
prior fluid loss. Replacement with crystalloid solutions should take into account:
--> maintenance fluid requirements
--> ongoing loss via the nasogastric tube
--> prior fluid loss including dehydration from prolonged vomiting
--> third-space loss into the peritoneal cavity and bowel lumen.
Elevation of the serum haematocrit and blood urea are useful indicators of the
degree of dehydration and third-space loss. The primary goals of fluid management are the
maintenance of a normal blood pressure and the establishment of an adequate urinary
output approaching 30 mL per hour. Rapid initial fluid replacement should include
crystalloid supplemented by colloid colutions and is monitored continuously against central
venous and pulmonary artery wedge pressures. If the haematocrit is low in the septic
patient, blood transfusion is an appropriate addition to crystalloids, both for replacement
and correction of anaemia.